Abstract
Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI. By gaining a deeper understanding of the mechanisms of cardiomyocyte death, it aims to provide new insights into the prevention and treatment of MI.
Published Version
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